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Genetics of Cardiovascular Disease series. Click the PLAY button below to watch the sample extract.
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Prof. Petri Kovanen - Wihuri Research Institute, Helsinki, Finland Petri Kovanen received his medical degree in 1970 from the University of Basel, Switzerland, and then his MD and PhD at the University of Helsinki, Finland. His main research interests focus on the pathogenesis of atherosclerosis, both early atherogenesis with an emphasis on the mechanisms of extracellular lipid accumulation, and late atherogenesis with emphasis on the generation of vulnerable plaques. Throughout the years, he has been studying the role of mast cells in atherogenesis, a rediscovered invader of the atherosclerotic arterial wall. Dr. Kovanen has written numerous scientific articles, reviews, and book chapters on topics dealing with the pathophysiology of atherosclerosis, with special emphasis on mast cells. Dr. Kovanen is the Editor-in-Chief of Annals of Medicine, and serves on the Editorial Board of Arteriosclerosis, Thrombosis, and Vascular Biology.
Talk Online Publication: Dec 2008 How to cite this talk:
Kovanen, P. (2008), "Plaque rupture", in Humphries, S. (ed.), Genetics of Cardiovascular Disease: Genetic interactions in a multifactorial disease, The Biomedical & Life Sciences Collection, Henry Stewart Talks Ltd, London (online at http://hstalks.com/bio)
Direct talk access link:
http://hstalks.com/lib.php?t=HST69.2159_1_2&c=252
TOPICS COVERED IN PLAQUE RUPTURE Inflammation and aetherosclerosis | Immune activation | Response to injury hypothesis | Discovery of the pathophysiology of aetherosclerosis | The cholesterol era | The LDL level | Arterial intima: the site of atherogenesis | Genesis of thickening intima | Adaptive intimal thickening | Topology of coronary athero-sclerotic lesions | Cholesterol in blood and in coronary arterial wall | The "bad" LDL cholesterol and the "good" HDL cholesterol: an imbalance | Coronary artery disease | LDL-driven atherosclerosis leads to coronary stenosis |Human coronary atheroma | Atherothrombosis | Plaque disruption | Structure of an LDL particle | Extracellular aggregated and fused LDL particles in the arterial intima of genetically hyperlipidemic mouse | Extracellular lipid droplets in human atherosclerotic plaque | Fatty streak formation in human fetal aortas is enchanced by maternal hypercholesterolemia | Transmigration of monocytes | Foam cells between cap and core of a coronary atheroma | Coronary fibroatheroma | LDL modification in the arterial intima: a vicious circle | Accumulation of LDL in the arterial intima | Mast cell neutral proteases activate MMPs | Degradation of collagen | Preventing cholesterol accumulation and subsequent inflammation or even more?
1. Introduction
2. Inflammation and atherosclerosis - an early start
3. Infection and atherosclerosis
4. Immune activation
5. Response to injury hypothesis
6. Inflammation - the 21st century hypothesis
7. Pathophysiology of atherosclerosis - cholesterol
8. 1914 - the start of the cholesterol era
9. It is the LDL level that counts
10. Arterial intima - the site of atherosclerosis
11. Genesis of thickening intima
12. Adaptive intimal thickening
13. Coronary athero-sclerotic lesions
14. Cholesterol in the blood and coronary arterial wall
15. Coronary artery disease
16. LDL-driven atherosclerosis - negative remodeling
17. Human coronary atheroma
18. LDL-driven atheroma - positive remodeling
19. Real life - both negative and positive remodeling
20. Atherothrombosis
21. Atherothrombosis - the final stage
22. Plaque disruption without luminal thrombosis
23. Plaque disruption - luminal mural thrombosis
24. Plaque disruption - infract related thrombosis
25. Structure of an LDL particle
26. Transcytosis of LDL particles
27. Extracellular matrix of the arterial intima
28. Accumulation of infused human LDL in rabbit
29. Fatty streak formation in fetal aortal intima
30. Adhesion of monocytes to plaque endothel
31. Transmigration of monocytes
32. Macrophage foam cells in the PG rich layer
33. Coronary fatty streak
34. Foam cell between the cap and core of atheroma
35. Coronary fibroatheroma
36. LDL modification in the arterial intima
37. Accumulation of LDL in the arterial intima
38. Oxidants/hydrolases accelerate LDL modification
39. Formation of an early atherosclerotic lesions
40. Regression of a foam cell into a macrophage
41. Lipid core formation
42. Degradation of collagen
43. Summary
44. END
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